Prognostic Significance of Acute Kidney Injury After Reperfused ST-Elevation Myocardial Infarction: Synergistic Acceleration of Renal Dysfunction and Left Ventricular Remodeling

Anzai, Atsushi; Anzai, Toshihisa; Naito, Kunihiko; Kaneko, Hidehiro; Mano, Yoshinori; Jo, Yusuke; Nagatomo, Yuji; Maekawa, Yuichiro; Kawamura, Akio; Yoshikawa, Tsutomu; Ogawa, Satoshi

doi:10.1016/j.cardfail.2009.12.020

Cited by 62 publications

(53 citation statements)

References 44 publications

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“…However, other pathophysiologic considerations include ongoing neurohormonal activation from excess diuresis and acute kidney injury. 23 Although we cannot infer from our data whether these trajectories are a marker or mediator of adverse outcomes, having this information available within 7 days may be helpful in targeting high-risk patients for closer follow-up and laboratory assessment. Heart failure readmission, particularly in the Medicare population, is associated with impaired survival and rising healthcare costs 21,24 ; and sobering data show that shorter hospitalization and lack of an early postdischarge visit are strong predictors of readmission.…”

Section: Discussionmentioning

confidence: 89%

Renal Function Trajectories and Clinical Outcomes in Acute Heart Failure

Givertz

Postmus

Hillege

et al. 2014

Circ: Heart Failure

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Background-Prior studies have demonstrated adverse risk associated with baseline and worsening renal function in acute heart failure, but none has modeled the trajectories of change in renal function and their impact on outcomes. Methods and Results-We used linear mixed models of serial measurements of blood urea nitrogen and creatinine to describe trajectories of renal function in 1962 patients with acute heart failure and renal dysfunction enrolled in the Placebo-Controlled Randomized Study of the Selective A 1 Adenosine Receptor Antagonist Rolofylline for Patients Hospitalized with Acute Decompensated Heart Failure and Volume Overload to Assess Treatment Effect on Congestion and Renal Function study. We assessed risk of 180-day mortality and 60-day cardiovascular or renal readmission and used Cox regression to determine association between renal trajectories and outcomes. Compared with patients alive at 180 days, patients who died were older, had lower blood pressure and ejection fraction, and higher creatinine levels at baseline. On average for the entire cohort, creatinine rose from days 1 to 3 and increased further after discharge, with the trajectory dependent on the day of discharge. Blood urea nitrogen, creatinine, and the rate of change in creatinine from baseline were the strongest independent predictors of 180-day mortality and 60-day readmission, whereas the rate of change of blood urea nitrogen from baseline was not predictive of outcomes. Baseline blood urea nitrogen >35 mg/ dL and increase in creatinine >0.1 mg/dL per day increased the risk of mortality, whereas stable or decreasing creatinine was associated with reduced risk. Conclusions-Patients with acute heart failure and renal dysfunction demonstrate variable rise and fall in renal indices during and immediately after hospitalization. Risk of morbidity and mortality can be predicted based on baseline renal function and creatinine trajectory during the first 7 days. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifiers: NCT00328692 and NCT00354458.(Circ Heart Fail. 2014;7:59-67.)

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Section: Discussionmentioning

confidence: 89%

Renal Function Trajectories and Clinical Outcomes in Acute Heart Failure

Givertz

Postmus

Hillege

et al. 2014

Circ: Heart Failure

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“…Even small acute changes in serum creatinine modify the risk of death [9]. Among those developing AKI, greater risk of cardiovascular events such as CHF, recurrent ACS, and stroke and need for re-hospitalization have been shown [9,28,29]. Newsome et al [7] reported a greater likelihood of progression to ESKD in those with ACS complicated by AKI.…”

Section: Introductionmentioning

confidence: 96%

“…After adjustment for covariates, AKI was independently associated with long-term mortality (HR 1.12, 95% CI, 1.04-1.20). AKI associated with ACS increases the risk of poor outcome [4,[7][8][9][27][28][29][30]. Even small acute changes in serum creatinine modify the risk of death [9].…”

Section: Introductionmentioning

confidence: 99%

Epidemiology and outcome of the cardio-renal syndrome

Cruz

Gheorghiade

Palazuolli³

et al. 2010

Heart Fail Rev

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Cardiac and kidney disease are common, increasingly encountered and often co-exist. Recently, the Acute Dialysis Quality Initiative (ADQI) Working Group convened a consensus conference to develop a classification scheme for the CRS and for five discrete subtypes. These CRS subtypes likely share pathophysiologic mechanisms, however, also have distinguishing clinical features, in terms of precipitating events, risk identification, natural history and outcomes. Knowledge of the epidemiology of heart-kidney interaction stratified by the proposed CRS subtypes is increasingly important for understanding the overall burden of disease for each CRS subtype, along with associated morbidity, mortality and health resource utilization. Likewise, an understanding of the epidemiology of CRS is necessary for characterizing whether there exists important knowledge gaps and to aid the in the design of clinical studies. In the most recent European and American guidelines for heart failure management, acute kidney injury and dysfunction were considered an index of poor prognosis. Paradoxically, however, in many randomized trials of interventions for patients with heart failure, those with kidney injury or dysfunction are often excluded. This review will provide a summary of the epidemiology of the cardio-renal syndrome and its subtypes.

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“…It has been also demonstrated that when an angiotensin II receptor antagonist was administered in a rat MI model, both expression of MCP-1 and macrophage infiltration in the border zone were reduced, 14 indicating the involvement of activation of the renin-angiotensin (RA) system in the promotion of inflammatory response. In chronic kidney disease patients with estimated glomerular filtration rate <60 ml · min -1 · 1.73 m -2 on admission 15 and those with the complication of so-called acute kidney injury (AKI) whose serum creatinine level increases to >0.3 mg/dl within 48 h of admission, 16 it is reported that peak CRP level increased concurrently with plasma interleukin (IL)-6 and serum malondialdehyde-modified low density lipoprotein (oxidized LDL) levels. Renal dysfunction may not only increase the production of inflammatory mediators, oxidative stressors and advanced glycation endproducts via activation of the RA system, but also activate inflammation by reducing the clearance of these substances.…”

Section: Modification Of Crp Elevation By Patient Demographic Factorsmentioning

confidence: 99%

Post-Infarction Inflammation and Left Ventricular Remodeling

Anzai

2013

Circ J

Self Cite

124

107

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp non-specific response to tissue damage. 1 However, an investigation into the relation between the peak body temperature during the first week and in-hospital complications since the event of MI showed that the incidence of complications of pump failure (grade of class 2 or greater according to Killip's classification or subset II or greater according to Forrester's classification) and ventricular aneurysm, as well as the incidence of cardiovascular events such as cardiac death, pump failure, fatal ventricular arrhythmias and cardiac rupture, increased in proportion to the body temperature increase. 2 Although the peak creatine kinase (CK) level, an indicator of infarct size, was similar, LV end-diastolic and LV end-systolic volumes measured by left ventriculography before discharge had increased and the LV ejection fraction decreased in proportion to the peak body temperature, demonstrating an association between body temperature increase after MI and LV remodeling. 2 Post-MI Inflammation and Infarct ExpansionDuring the acute phase of MI, resident macrophages in the myocardial tissue are activated following neutrophil infiltration into the infarcted region. CD11b/18 on the surface of neutroeft ventricular (LV) remodeling after myocardial infarction (MI) is the process of infarct expansion followed by non-infarct hypertrophy and progressive LV dilation, and is associated with adverse clinical outcomes. Defective infarct healing, as well as infarct size and wall stress, is a major determinant of infarct expansion. A well-orchestrated inflammatory response after MI leads to an appropriate infarct healing process and formation of a scar with tensile strength, preventing infarct expansion. Despite the importance of the inflammatory response and healing process in post-MI LV remodeling, the mechanisms that initiate and control these processes have not been fully elucidated. Numerous clinical and experimental studies have focused on the role of inflammation and its regulatory mechanism as a novel therapeutic target for post-infarction LV remodeling. Increase in Body Temperature and Post-MI ComplicationsThe 4 classical signs of inflammation are dolor, tumor, rubor and calor. It has also been recognized for a long time that body temperature increases after MI, reflecting the development of inflammation after tissue necrosis, but it was believed to be a After myocardial infarction (MI), inflammatory cells such as neutrophils, followed by monocytes and macrophages, infiltrate and phagocytose the necrotic tissues, as well as secreting a variety of inflammatory cytokines. The vulnerable myocardium, which consists of necrotic tissue and inflammatory cells, is susceptible to wall stress, resulting in infarct expansion. Subacute cardiac rupture is an extreme form of infarct expansion, whereas ventricular aneurysm is its chronic form and a trigger for subsequent left ventricular (LV) remodeling. Although post-infarction inflammation...

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Prognostic Significance of Acute Kidney Injury After Reperfused ST-Elevation Myocardial Infarction: Synergistic Acceleration of Renal Dysfunction and Left Ventricular Remodeling

Cited by 62 publications

References 44 publications

Renal Function Trajectories and Clinical Outcomes in Acute Heart Failure

Renal Function Trajectories and Clinical Outcomes in Acute Heart Failure

Epidemiology and outcome of the cardio-renal syndrome

Post-Infarction Inflammation and Left Ventricular Remodeling

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